Novel Nanocombinations of L-tryptophan and L-cysteine: Preparation, Characterization and Their Applications for Dye Decolorization, Antimicrobial and Anticancer Activities

2021 ◽  
Author(s):  
Ahmed I. Abd-Elhamid ◽  
Hamada El-Gendi ◽  
Abdallah E. Abdallah ◽  
Esmail El-Fakharany
Keyword(s):  
Cancer Cells ◽  
Dye Removal ◽  
P53 Gene ◽  
Dye Decolorization ◽  
Dependent Manner ◽  
Anticancer Activities ◽  
Acid Modification ◽  
Potent Effect ◽  
Noticeable Improvement ◽  
Cation Exchange Column

Abstract Tungsten oxide WO3 nanoparticles (NPs) were prepared in a form of nanosheets with a homogeneous size and dimensions in one step through acid precipitation using a cation exchange column. The resulting WO3 nanosheets surface was decorated with one of the two amino acids (AAs) L-tryptophan (Trp) or L-cysteine (Cys) for their dye removal, antimicrobial, and antitumor activities. A noticeable improvement in the biological activity of WO3 NPs was detected upon amino acid modification compared to the original WO3. The prepared WO3-Trp and WO3-Cys exhibited strong dye removal activity toward methylene blue and safranin dyes with complete dye removal (100%) after 6 h. WO3-Cys NPs and WO3-Trp NPs revealed higher broad-spectrum antibacterial activity toward both G-ve and G+ve bacteria with strong antifungal activity toward Candida albicans. Anticancer results of the modified WO3-Cys and WO3-Trp NPs against various kinds of cancer cells including MCF-7, caco-2, and HepG-2 cells indicated that they have a potent effect in a dose-dependent manner with high selectivity to cancer cells and safety against normal cells. The expression levels of E2F2, Bcl-2 genes were found to be suppressed after treatment with both WO3-Cys and WO3-Trp NPs more than 5-FU-treated cells. While expression level of the p53 gene in all tested cells was evidently up-regulated after treatment by more than 5-8 folds as compared to untreated cells. The docking results confirmed the ability of both NPs to bind to P53 gene with relevant potency in binding to other tested gens and participation of cysteine SH-functional group in such interaction.

scholarly journals Novel Nanocombinations of l-Tryptophan and l-Cysteine: Preparation, Characterization, and Their Applications for Antimicrobial and Anticancer Activities

Pharmaceutics ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 1595
Author(s):  
Ahmed I. Abd-Elhamid ◽  
Hamada El-Gendi ◽  
Abdallah E. Abdallah ◽  
Esmail M. El-Fakharany
Keyword(s):  
Cancer Cells ◽  
Dye Removal ◽  
P53 Gene ◽  
Dependent Manner ◽  
Anticancer Activities ◽  
Acid Modification ◽  
Potent Effect ◽  
Amino Acid Modification ◽  
Noticeable Improvement ◽  
Cation Exchange Column

Tungsten oxide WO3 nanoparticles (NPs) were prepared in a form of nanosheets with homogeneous size and dimensions in one step through acid precipitation using a cation exchange column. The resulting WO3nanosheet surface was decorated with one of the two amino acids (AAs) l-tryptophan (Trp) or l-cysteine (Cys) and evaluated for their dye removal, antimicrobial, and antitumor activities. A noticeable improvement in the biological activity of WO3 NPs was detected upon amino acid modification compared to the original WO3. The prepared WO3-Trp and WO3-Cys exhibited strong dye removal activity toward methylene blue and safranin dyes with complete dye removal (100%) after 6 h. WO3-Cys and WO3-Trp NPs revealed higher broad-spectrum antibacterial activity toward both Gram-negative and Gram-positive bacteria, with strong antifungal activity toward Candida albicans. Anticancer results of the modified WO3-Cys and WO3-Trp NPs against various kinds of cancer cells, including MCF-7, Caco-2, and HepG-2 cells, indicate that they have a potent effect in a dose-dependent manner with high selectivity to cancer cells and safety against normal cells. The expression levels of E2F2 and Bcl-2 genes were found to be suppressed after treatment with both WO3-Cys and WO3-Trp NPs more than 5-FU-treated cells. While expression level of the p53 gene in all tested cells was up-regulated after treatment 5–8 folds more as compared to untreated cells. The docking results confirmed the ability of both NPs to bind to the p53 gene with relevant potency in binding to other tested gens and participation of cysteine SH-functional group in such interaction.

scholarly journals NBM-HD-1: A Novel Histone Deacetylase Inhibitor with Anticancer Activity

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Wei-Jan Huang ◽  
Yu-Chih Liang ◽  
Shuang-En Chuang ◽  
Li-Ling Chi ◽  
Chi-Yun Lee ◽  
...  
Keyword(s):  
Anticancer Activity ◽  
Cancer Cells ◽  
Anticancer Agents ◽  
Xenograft Model ◽  
Cyclin B1 ◽  
Dependent Manner ◽  
Cell Cycle Regulators ◽  
Anticancer Activities ◽  
Gene Expressions

HDAC inhibitors (HDACis) have been developed as promising anticancer agents in recent years. In this study, we synthesized and characterized a novel HDACi, termed NBM-HD-1. This agent was derived from the semisynthesis of propolin G, isolated from Taiwanese green propolis (TGP), and was shown to be a potent suppressor of tumor cell growth in human breast cancer cells (MCF-7 and MDA-MB-231) and rat glioma cells (C6), with an IC50ranging from 8.5 to 10.3 μM. Western blot demonstrated that levels of p21(Waf1/Cip1), gelsolin, Ac-histone 4, and Ac-tubulin markedly increased after treatment of cancer cells with NBM-HD-1. After NBM-HD-1 treatment for 1–4 h, p-PTEN and p-AKT levels were markedly decreased. Furthermore, we also found the anticancer activities of NBM-HD-1 in regulating cell cycle regulators. Treatment with NBM-HD-1,p21(Waf1/Cip1)gene expression had markedly increased whilecyclin B1andD1gene expressions had markedly decreased. On the other hand, we found that NBM-HD-1 increased the expressions of tumor-suppressor genep53in a dose-dependent manner. Finally, we showed that NBM-HD-1 exhibited potent antitumor activity in a xenograft model. In conclusion, this study demonstrated that this compound, NBM-HD-1, is a novel and potent HDACi with anticancer activityin vitroandin vivo.

scholarly journals Orphan Receptor COUP-TF Is Required for Induction of Retinoic Acid Receptor β, Growth Inhibition, and Apoptosis by Retinoic Acid in Cancer Cells

2000 ◽  
Vol 20 (3) ◽  
pp. 957-970 ◽  
Author(s):  
Bingzhen Lin ◽  
Guo-quan Chen ◽  
Dongmei Xiao ◽  
Siva Kumar Kolluri ◽  
Xihua Cao ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Retinoic Acid Receptor ◽  
Critical Role ◽  
Orphan Receptor ◽  
Dependent Manner ◽  
Anticancer Activities ◽  
Transient Transfection Assay ◽  
Acid Receptor

ABSTRACT Retinoic acid receptor β (RARβ) plays a critical role in mediating the anticancer effects of retinoids. Expression of RARβ is highly induced by retinoic acid (RA) through a RA response element (βRARE) that is activated by heterodimers of RARs and retinoid X receptors (RXRs). However, RARβ induction is often lost in cancer cells despite expression of RARs and RXRs. In this study, we provide evidence that orphan receptor COUP-TF is required for induction of RARβ expression, growth inhibition, and apoptosis by RA in cancer cells. Expression of COUP-TF correlates with RARβ induction in a variety of cancer cell lines. In addition, stable expression of COUP-TF in COUP-TF-negative cancer cells restores induction of RARβ expression, growth inhibition, and apoptosis by RA, whereas inhibition of COUP-TF by expression of COUP-TF antisense RNA represses the RA effects. In a transient transfection assay, COUP-TF strongly induced transcriptional activity of the RARβ promoter in a RA- and RARα-dependent manner. By mutation analysis, we demonstrate that the effect of COUP-TF requires its binding to a DR-8 element present in the RARβ promoter. The binding of COUP-TF to the DR-8 element synergistically increases the RA-dependent RARα transactivation function by enhancing the interaction of RARα with its coactivator CREB binding protein. These results demonstrate that COUP-TF, by serving as an accessory protein for RARα to induce RARβ expression, plays a critical role in regulating the anticancer activities of retinoids.

scholarly journals Effect of Calomelanone, a Dihydrochalcone Analogue, on Human Cancer Apoptosis/Regulated Cell Death in an In Vitro Model

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Wasitta Rachakhom ◽  
Ratana Banjerdpongchai
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Hepg2 Cells ◽  
Cytotoxic Effect ◽  
Human Cancer ◽  
Autophagic Flux ◽  
Dependent Manner ◽  
Anticancer Activities ◽  
Human Cancer Cells ◽  
Regulated Cell Death

Calomelanone, 2 ′ ,6 ′ -dihydroxy-4,4 ′ -dimethoxydihydrochalcone, possesses anticancer activities. This study was conducted to investigate the cytotoxic effect of calomelanone, a dihydrochalcone analogue, on human cancer cells and its associated mechanisms. The cytotoxic effect of calomelanone was measured by MTT assay. Annexin V-FITC/propidium iodide and DiOC6 staining that employed flow cytometry were used to determine the mode of cell death and reduction of mitochondrial transmembrane potential (MTP), respectively. Caspase activities were measured using specific substrates and colorimetric analysis. The expression levels of Bcl-2 family proteins were determined by immunoblotting. Reactive oxygen species were also measured using 2 ′ ,7 ′ -dihydrodichlorofluorescein diacetate and dihydroethidium (fluorescence dyes). Calomelanone was found to be toxic towards various human cancer cells, including acute promyelocytic HL-60 and monocytic leukemic U937 cells, in a dose-dependent manner at 24 h and human hepatocellular HepG2 cells at 48 h. However, the proliferation of HepG2 cells increased at 24 h. Calomelanone was found to induce apoptosis in HL-60 and U937 at 24 h and HepG2 apoptosis at 48 h via the intrinsic pathway by inducing MTP disruption. This compound also induced caspase-3, caspase-8, and caspase-9 activities. Calomelanone upregulated proapoptotic Bax and Bak and downregulated antiapoptotic Bcl-xL proteins in HepG2 cells. Moreover, signaling was also associated with oxidative stress in HepG2 cells. Calomelanone induced autophagy at 24 h of treatment, which was evidenced by staining with monodansylcadaverine (MDC) to represent autophagic flux. This was associated with a decrease of Akt (survival pathway) and an upregulation of Atg5 (the marker of autophagy). Thus, calomelanone induced apoptosis/regulated cell death in HL-60, U937, and HepG2 cells. However, it also induced autophagy in HepG2 depending on duration, dose, and type of cells. Thus, calomelanone could be used as a potential anticancer agent for cancer treatment. Nevertheless, acute and chronic toxicity should be further investigated in animals before conducting investigations in human patients.

scholarly journals Cytotoxic activities of zinc oxide nanoparticles on non-invasive human breast and prostate cancer cell lines

2021 ◽  
Vol 12 (1) ◽  
pp. 749-756
Author(s):  
Fakhria A Al-joufi ◽  
Jawaher AlEnzi ◽  
Madawy Alhazmi ◽  
Hassan A Elgebaly
Keyword(s):  
Zinc Oxide ◽  
Cancer Cells ◽  
Sol Gel ◽  
Research Work ◽  
Cytotoxic Activities ◽  
Dependent Manner ◽  
Anticancer Activities ◽  
Zno Nps ◽  
Gel Method ◽  
Sol Gel Method

ZnO-NPs have displayed anticancer activity against a broad range of tumor cells. The present research work was planned to formulate highly pure and well-characterized ZnO-NPs, in addition, to investigate their cytotoxicity against two types of cancer cells. The cancer cells that had been investigated in the present study were breast (MCF7) and prostate (PC3) cancer cells. The aqueous sol-gel method is a powerful and cost-effective technique for the synthesis of high pure ZnO-NPs. While the anticancer activities of ZnO-NPs on both MCF7 and PC3 were determined by MTT assay. Characterizations of ZnO-NPs were fundamentally evaluated by their morphological and structural properties, in addition to their particle size distribution with the aid of SEM and EDX, respectively. ZnO NPs were successfully prepared using sol-gel method in a range of nano-scale. Scanning electron microscopy (SEM) has shown flower-like nanoparticles of zinc oxide, their nano-size has ranged from 4.497 nm. to 143.7 nm. Results of EDX characterization has exhibited a good purity of ZnO-NPs (zinc content of 50% and Oxygen content of 50 %). There was size-dependent effectiveness of ZnO-NPs as an anticancer agent on both MCF7 and PC3. In addition, there were positive correlation between anticancer activities and low toxicity with the size of ZnO-NPs. At 12.2 μg/ml, ZnO-NPs has exhibited around 51% reduction in the viability of cancerous cells. In conclusion, the results of this study have shown that there was an effective and notable dose-dependent manner in the treatment of MCF7 and PC3 with ZnO-NPs, in the cell line approaches. 

scholarly journals Semecarpus anacardium Linn. leaf extract exhibits activities against breast cancer and prolongs the survival of tumor bearing mice

2020 ◽  
Author(s):  
Rajesh Kumar Singh ◽  
Amit Ranjan ◽  
Ruchita Tripathi ◽  
Sumit Singh Verma ◽  
Vinamra Sharma ◽  
...  
Keyword(s):  
Ethyl Acetate ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ethyl Acetate Extract ◽  
Dependent Manner ◽  
Microbial Infection ◽  
Mice Model ◽  
Anticancer Activities ◽  
Semecarpus Anacardium ◽  
Tumor Bearing

ABSTRACTSemecarpus anacardium Linn. is a commonly used Ayurvedic medicinal plant which nuts have been described in Ayurveda and Sidda system of medicine to treat clinical ailments such as vitiligo, inflamation, microbial infection, geriatric problem, baldness and neuro related problems. In this study, anti-cancer activity of the leaves of Semecarpus anacardium Linn was evaluated for future drug development. The phytochemical screening was done by GC-MS analysis, cytotoxicity was examined using MTT assay, mode of cell death was evaluated by fluorescence microscopy and finally antitumor activity was determined in EAC cell induced tumor bearing mice. The ethyl acetate extract from the leaves of the plant induced cytotoxicity in cancer cells in a dose dependent manner (IC50: 0.57 μg/ml in MCF-7 cells) in different cancer cell lines. The non-malignant cells were relatively insensitive to the extract. The staining with acridine orange, ethidium bromide and DAPI confirmed that the extract induced apoptosis in cancer cells. Furthermore, the extract induced cell cycle arrest at G1 phase and suppressed cancer cell migration. An oral administration of the extract suppressed the tumor growth in mice model bearing ehrlich ascites carcinoma cells. The ethyl acetate extract was also found to prolong the survival of tumor bearing mice.Overall, these observations suggest the anticancer activities of the ethyl acetate extract of the leaves of S. anacardium. The study opens a new window to examine the phytochemical constituents from the leaves of the plant responsible for the anticancer activities.

scholarly journals Semecarpus Anacardium Linn. Leaf Extract Exhibits Activities Against Breast Cancer And Prolongs The Survival of Tumor Bearing Mice

2021 ◽  
Author(s):  
Rajesh Kumar Singh ◽  
Amit Ranjan ◽  
Ruchita Tripathi ◽  
Sumit Singh Verma ◽  
Vinamra Sharma ◽  
...  
Keyword(s):  
Ethyl Acetate ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Ethyl Acetate Extract ◽  
Dependent Manner ◽  
Microbial Infection ◽  
Mice Model ◽  
Anticancer Activities ◽  
Semecarpus Anacardium ◽  
Tumor Bearing

Abstract Semecarpus anacardium Linn. is a commonly used Ayurvedic medicinal plant which nuts have been described in Ayurveda and Sidda system of medicine to treat clinical ailments such as vitiligo, inflamation, microbial infection, geriatric problem, baldness and neuro related problems. In this study, anti-cancer activity of the leaves of Semecarpus anacardium Linn was evaluated for future drug development. The phytochemical screening was done by GC-MS analysis, cytotoxicity was examined using MTT assay, mode of cell death was evaluated by fluorescence microscopy and finally antitumor activity was determined in EAC cell induced tumor bearing mice. The ethyl acetate extract from the leaves of the plant induced cytotoxicity in cancer cells in a dose dependent manner (IC50: 0.57 µg/ml in MCF-7 cells) in different cancer cell lines. The non-malignant cells were relatively insensitive to the extract. The staining with acridine orange, ethidium bromide and DAPI confirmed that the extract induced apoptosis in cancer cells. Furthermore, the extract induced cell cycle arrest at G1 phase and suppressed cancer cell migration. An oral administration of the extract suppressed the tumor growth in mice model bearing ehrlich ascites carcinoma cells. The ethyl acetate extract was also found to prolong the survival of tumor bearing mice. Overall, these observations suggest the anticancer activities of the ethyl acetate extract of the leaves of S. anacardium. The study opens a new window to examine the phytochemical constituents from the leaves of the plant responsible for the anticancer activities.

scholarly journals The Indolic Diet-Derivative, 3,3′-Diindolylmethane, Induced Apoptosis in Human Colon Cancer Cells through Upregulation of NDRG1

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
A. Lerner ◽  
M. Grafi-Cohen ◽  
T. Napso ◽  
N. Azzam ◽  
F. Fares
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Colonic Cancer ◽  
P53 Gene ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Hct 116 ◽  
Poorly Differentiated ◽  
Induced Apoptosis

N-myc downstream regulated gene-1 participates in carcinogenesis, angiogenesis, metastases, and anticancer drug resistance. In the present study, we analyzed the expression pattern of N-myc downstream regulated gene-1 following treatment of human colonic cancer cell lines; HCT-116 (well differentiated with wild-type p53 gene) and Colo-320 (poorly differentiated with mutant p53 gene), with 3,3′-diindolylmethane, a well-established proapoptotic agent product derived from indole-3-carbinol. Treatment of Colo-320 and HCT-116 with 3,3′-diindolylmethane disclosed inhibition of cell viability in a dose-dependent manner, mediated through apoptosis induction. The increased expression of N-myc downstream regulated gene-1 was detected only in poorly differentiated colon cancer cells, Colo-320 cell line. Our results suggest that N-myc downstream regulated gene-1 expression is enhanced by 3,3′-diindolylmethane in poorly differentiated cells and followed by induction of apoptosis. 3,3′-diindolylmethane induced apoptosis may represent a new regulator of N-myc downstream regulated gene-1 in poorly differentiated colonic cancer cells.

Non-canonical Functions of Telomerase Reverse Transcriptase: Emerging Roles and Biological Relevance

2020 ◽  
Vol 20 (6) ◽  
pp. 498-507 ◽  
Author(s):  
Connor A.H. Thompson ◽  
Judy M.Y. Wong
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Reverse Transcriptase ◽  
Cancer Cells ◽  
Telomere Length ◽  
Telomere Maintenance ◽  
Telomerase Reverse Transcriptase ◽  
Alternative Mechanism ◽  
Dependent Manner ◽  
Mitochondrial Integrity

Increasing evidence from research on telomerase suggests that in addition to its catalytic telomere repeat synthesis activity, telomerase may have other biologically important functions. The canonical roles of telomerase are at the telomere ends where they elongate telomeres and maintain genomic stability and cellular lifespan. The catalytic protein component Telomerase Reverse Transcriptase (TERT) is preferentially expressed at high levels in cancer cells despite the existence of an alternative mechanism for telomere maintenance (alternative lengthening of telomeres or ALT). TERT is also expressed at higher levels than necessary for maintaining functional telomere length, suggesting other possible adaptive functions. Emerging non-canonical roles of TERT include regulation of non-telomeric DNA damage responses, promotion of cell growth and proliferation, acceleration of cell cycle kinetics, and control of mitochondrial integrity following oxidative stress. Non-canonical activities of TERT primarily show cellular protective effects, and nuclear TERT has been shown to protect against cell death following double-stranded DNA damage, independent of its role in telomere length maintenance. TERT has been suggested to act as a chromatin modulator and participate in the transcriptional regulation of gene expression. TERT has also been reported to regulate transcript levels through an RNA-dependent RNA Polymerase (RdRP) activity and produce siRNAs in a Dicer-dependent manner. At the mitochondria, TERT is suggested to protect against oxidative stress-induced mtDNA damage and promote mitochondrial integrity. These extra-telomeric functions of TERT may be advantageous in the context of increased proliferation and metabolic stress often found in rapidly-dividing cancer cells. Understanding the spectrum of non-canonical functions of telomerase may have important implications for the rational design of anti-cancer chemotherapeutic drugs.

Sign in / Sign up

Export Citation Format

Share Document